Accreting coral reefs in a highly urbanized environment

Globally, many coral reefs have fallen into negative carbonate budget states, where biological erosion exceeds carbonate production. The compounding effects of urbanization and climate change have caused reductions in coral cover and shifts in community composition that may limit the ability of reefs to maintain rates of vertical accretion in line with rising sea levels. Here we report on coral reef carbonate budget surveys across seven coral reefs in Singapore, which persist under chronic turbidity and in highly disturbed environmental conditions, with less than 20% light penetration to 2 m depth. Results show that mean net carbonate budgets across Singapore’s reefs were relatively low, at 0.63 ± 0.27 kg CaCO3 m−2 yr−1 (mean ± 1 SE) with a range from − 1.56 to 1.97, compared with the mean carbonate budgets across the Indo-Pacific of 1.4 ± 0.15 kg CaCO3 m−2 yr−1, and isolated Indian Ocean reefs pre-2016 bleaching (~ 3.7 kg CaCO3 m−2 yr−1). Of the seven reefs surveyed, only one reef had a net negative, or erosional budget, due to near total loss of coral cover (\u3c 5% remaining coral). Mean gross carbonate production on Singapore’s reefs was dominated by stress-tolerant and generalist species, with low-profile morphologies, and was ~ 3 kg m−2 yr−1 lower than on reefs with equivalent coral cover elsewhere in the Indo-Pacific. While overall these reefs are maintaining and adding carbonate structure, their mean vertical accretion potential is below both current rates of sea level rise (1993–2010), and future predictions under RCP 4.5 and RCP 8.5 scenarios. This is likely to result in an increase of 0.2–0.6 m of water above Singapore’s reefs in the next 80 yr, further narrowing the depth range over which these reefs can persist

Growth and carbonate production of crustose coralline algae on a degraded turbid reef system

Crustose coralline algae (CCA) and other encrusting calcifiers drive carbonate production on coral reefs. However, little is known about the rates of growth and calcification of these organisms within degraded turbid reef systems. Here we deployed settlement cards (N = 764) across seven reefs in Singapore for two years to examine spatio-temporal variation in encrusting community composition and CCA carbonate production. Our results showed that CCA was the dominant encrusting taxa (63.7% ± 18.3SD) across reefs. CCA carbonate production rates (0.009–0.052 g cm−2 yr−1) were less than half of those reported for most Indo-Pacific reefs, but similar to other turbid reef systems. Highest CCA carbonate production rates were observed furthest from Singapore\u27s main shipping port, due to a relative increase in CCA cover on the offshore reefs. Our results suggest that proximity to areas of high industrialisation and ship traffic may reduce the cover of encrusting calcifying organisms and CCA production rates which may have negative, long-term implications for the stabilisation of nearshore reefs in urbanised settings

Weed Control Recommendations in Wheat

24 pp., 7 tables, 2 figuresThis publication offers suggestions for controlling weeds in wheat using cultural, mechanical and chemical methods

Performance of PCA3 and TMPRSS2:ERG urinary biomarkers in prediction of biopsy outcome in the Canary Prostate Active Surveillance Study (PASS).

BackgroundFor men on active surveillance for prostate cancer, biomarkers may improve prediction of reclassification to higher grade or volume cancer. This study examined the association of urinary PCA3 and TMPRSS2:ERG (T2:ERG) with biopsy-based reclassification.MethodsUrine was collected at baseline, 6, 12, and 24 months in the multi-institutional Canary Prostate Active Surveillance Study (PASS), and PCA3 and T2:ERG levels were quantitated. Reclassification was an increase in Gleason score or ratio of biopsy cores with cancer to ≥34%. The association of biomarker scores, adjusted for common clinical variables, with short- and long-term reclassification was evaluated. Discriminatory capacity of models with clinical variables alone or with biomarkers was assessed using receiver operating characteristic (ROC) curves and decision curve analysis (DCA).ResultsSeven hundred and eighty-two men contributed 2069 urine specimens. After adjusting for PSA, prostate size, and ratio of biopsy cores with cancer, PCA3 but not T2:ERG was associated with short-term reclassification at the first surveillance biopsy (OR = 1.3; 95% CI 1.0-1.7, p = 0.02). The addition of PCA3 to a model with clinical variables improved area under the curve from 0.743 to 0.753 and increased net benefit minimally. After adjusting for clinical variables, neither marker nor marker kinetics was associated with time to reclassification in subsequent biopsies.ConclusionsPCA3 but not T2:ERG was associated with cancer reclassification in the first surveillance biopsy but has negligible improvement over clinical variables alone in ROC or DCA analyses. Neither marker was associated with reclassification in subsequent biopsies

Growth Arrest‐Specific 6 (GAS6) Promotes Prostate Cancer Survival by G1 Arrest/S Phase Delay and Inhibition of Apoptosis During Chemotherapy in Bone Marrow

Prostate cancer (PCa) is known to develop resistance to chemotherapy. Growth arrest‐specific 6 (GAS6), plays a role in tumor progression by regulating growth in many cancers. Here, we explored how GAS6 regulates the cell cycle and apoptosis of PCa cells in response to chemotherapy. We found that GAS6 is sufficient to significantly increase the fraction of cells in G1 and the duration of phase in PCa cells. Importantly, the effect of GAS6 on G1 is potentiated during docetaxel chemotherapy. GAS6 altered the levels of several key cell cycle regulators, including the downregulation of Cyclin B1 (G2/M phase), CDC25A, Cyclin E1, and CDK2 (S phase entry), while the upregulation of cell cycle inhibitors p27 and p21, Cyclin D1, and CDK4. Importantly, these changes became further accentuated during docetaxel treatment in the presence of GAS6. Moreover, GAS6 alters the apoptotic response of PCa cells during docetaxel chemotherapy. Docetaxel induced PCa cell apoptosis is efficiently suppressed in PCa cell culture in the presence of GAS6 or GAS6 secreted from co‐cultured osteoblasts. Similarly, the GAS6‐expressing bone environment protects PCa cells from apoptosis within primary tumors in vivo studies. Docetaxel induced significant levels of Caspase‐3 and PARP cleavage in PCa cells, while GAS6 protected PCa cells from docetaxel‐induced apoptotic signaling. Together, these data suggest that GAS6, expressed by osteoblasts in the bone marrow, plays a significant role in the regulation of PCa cell survival during chemotherapy, which will have important implications for targeting metastatic disease. J. Cell. Biochem. 117: 2815–2824, 2016. © 2016 Wiley Periodicals, Inc.We explored how GAS6, expressed by osteoblasts, regulates the cell cycle and apoptosis in PCa cells during chemotherapy in the bone marrow. We demonstrate that GAS6 significantly increases the number of G1 arrested cells by altering signaling networks associated with G1 arrest and S phase delay. Our results suggest that GAS6 contributes to the regulation of PCa cell survival during chemotherapy in the bone marrow microenvironment.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/134410/1/jcb25582_am.pdfhttp://deepblue.lib.umich.edu/bitstream/2027.42/134410/2/jcb25582.pd